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• Drought-tolerant and drought-sensitive accessions of cultivated and wild rice were used to investigate the mechanisms of drought tolerance. • Differentially expressed genes (DEGs) between the drought-treated and control samples and their co-expression patterns were analyzed. • Specific transcript factors and genes were identified to be associated with drought tolerance, with some of them being unique to wild rice. • There were clusters or hotspots of DEGs in which overrepresentation of the QTLs published previously were observed. Whole transcriptomic sequencing of the drought-tolerant (DT) and drought-sensitive (DS) accessions of cultivated and wild rice under drought treatments was performed to uncover the mechanism of plant adaptation to drought and to facilitate the development of drought-tolerant cultivars in crops. By analyzing the differentially expressed genes (DEGs) between the drought-treated and untreated samples and their co-expressed pattern, we revealed distinct susceptibilities of different samples to the stress treatments and identified some specific transcription factors (TFs) and genes that play critical roles in rice adaptation to drought. Some drought-responsive genes or pathways unique to the wild rice were also detected, highlighting the importance of wild rice resources in developing elite cultivars. Furthermore, we showed that the DEGs in the DT accessions were enriched in the genome as clusters or hotspots in which previously identified drought-associated quantitative trait loci (QTLs) were overrepresented. The finding that a single hotspot contained up to 52 QTLs and involved as many as 20 traits implicates the complicated genetic architecture underlying the DT traits. These results provide new insights into the understanding of plant adaptation to drought and help effective manipulation of specific genes or gene cluster in crop breeding. [ABSTRACT FROM AUTHOR]

Serum response factor (SRF), a transcription factor highly expressed in neurons, is involved in neuronal survival and the pathogenesis of some neurodegenerative disorders. The ablation of SRF renders the midbrain dopaminergic (DA) neurons vulnerable to 1-methyl 4-phenyl 1,2,3,6-tetrahydropyridine-induced neurotoxicity, however, the underlying mechanisms remain poorly understood. Here, we report decreased SRF levels in the substantia nigra (SN) of rotenone-treated rats that was associated with the loss of tyrosine hydroxylase (TH)-positive neurons. SRF expression was also reduced in rotenone-treated PC12 cells in vitro . In addition, Srf knockdown augmented rotenone-induced toxicity in PC12 cells. In contrast, overexpression of Srf attenuated the cells’ sensitivity to rotenone and alleviated rotenone-induced α-synuclein accumulation. The protective effect of SRF was abolished when the expression of autophagy-related proteins Beclin 1 and Atg5 was suppressed. These results suggested that SRF may promote DA neuron survival by regulating autophagy, and thus serves as a critical molecule in PD progression. [ABSTRACT FROM AUTHOR]